Course: Pathophys II Date: July 4, 2008 Class #: 11

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1 Course: Pathophys II Date: July 4, 2008 Class #: 11 Essay questions: Define and compare systolic and diastolic bp, mean arterial pressure and pulse pressure. Relate these to disease processes for more points. Describe (or compare/contrast) o asthma (thickening of bronch wall, reactive broncho constriction triggered by _, that it s an inflammatory process, etc.) o chronic bronchitis (disease of the airways/bronchi) o pneumonia (focus on disease of alveoli, most are infectious/viral) o autoimmune lung disease (many types, strong genetic component, all result in loss of lung elasticity) o emphysema o tuberculosis o pneumoconiosis (condit in which an enviro trigger gets into lungs and cause a chronic inflamm resulting in a stiffening of the lungs, longterm pulmonary insufficiency). (define them let him know I know what he s talking about. Compare and contrast them to help get jumpstarted. ) Atherosclerosis will be covered in m/c questions risk factors, how it contribs to coronary artery disease, stroke, peripheral vascular disease. Two sections not covered and not tested: kidney function and maintenance of normal electrolyte levels (esp sodium, potassium, phosphorous, minerals) and maintenance of blood ph kidney plays a large role in maintaining normal ph levels. Nothing on reproductive system either. 4 essays for extra credit plus one more he s not going to cover. M/C, fill in the blank, T/F questions are the rest of the test and will go over them next week before the test. Today s fun topics: endocrine system, pain and headache, nervous sytem Page 1 of 9

2 Chapter 42 pdf file Endocrine System Begins at hypothalamus, part of the midbrain. Regulator of bodily funx. Communic directly with the anterior pituitary. The anterior pituitary is a mixture of gland and brain a transition zone between the brain and endocrine. The hypothalamus is the master regulator. The pituitary coordinates endocrine feedback and hypothalamic input and acts accordingly. The pituitary oversees the extracranial components of the endocrine system. The master gland is the thyroid. It determines the rate at which metabolism happens. Hypothalamus Thyroid releasing hormone (TRH) ant pituitary to release of thyroid stimulating hormone which triggers the thyroid to release T3 and 4 from the follicular cells. 2 major funx of thyroid hormone: 1. Promotes growth, coordinating with growth hormone 2. Increases metabolism, breaks down fats, increases protein synthesis, use of glucose, fat, protein, mobilization of lipids, enhances catabolism of cholesterol in liver. Most active form of hormone is T3. T4 is the storage type and is converted to T3 in the peripheral tissues at the cellular level, not in the blood stream. Important because we need a large volume of circulating storage capacity T3 is used up very quickly. This way the cells that need the higher level have it on tap. The thyroid itself doesn t have to manufacture upon demand this way. Some patients have trouble converting it those with autoimmune thyroiditis for example (more common in women than men, no specific age range). Blood tests show normal to high T4 levels, but functionally they are hypothyroid because they cannot convert to the active form. More commonly, there is an absolute lack of T4 production in the thyroid gland. For these patients, you supplement them with T4 that can then be coverted to T3 as needed by the body. KNOW: control of prod/release of T4 is negative feedback (inhibition) to both the hypothalamus and pituitary gland. When levels are high, anterior hypothalamus will stop production until needed again. High T4 levels = reduction of TSH by pit/hypothalamus = lower T levels as T4 is converted to T3. Effect on metabolism Increases cardiovascular and gastrointestinal function. Also ups the activity of the sympathetic nervous system. The increase in the nervous system expresses as tremors, racing heart and all the other fun stuff adrenaline causes. Sleeplessness, increased metabolism, weight loss, increased perspiration. Different between T3 and T4 is that T4 has more iodine. When T4 is converted, one of the iodine modules is removed. Thus a common cause of hypothyroidism is a lack of iodine and thus an inability to make the needed T4. Page 2 of 9

3 Hypothyroidism Cretinism is congenital hypothyroidism, untreated. As thyroid hormone is essential for brain growth and development if left untreated the effects are life long. Primary hypo (most common): Thyoid not functioning. Affects almost all organ systems. Hypometabolic state. Lethargy, non-regenerative sleep, tired all the time. Myxedematous changes in tissues intracellular fluid accumulation (not outside of the cells pitting edema--, but inside of the cells non-pitting edema.) Skin gets thick, leathery and very dry. Cardinal sign of myxedema. Myxedema = non-pitting, mucous type in connective tissues, a late stage manifestation. Puffy appearance, esp eyes. Enlarged tongue and hoarseness. Hashimodo s thyroiditis is an autoimmune condition and is the most common cause of primary hypothyroidism. The thyroid gland is destroyed by anti-thyroid antibodies. There is a transient hyperthyroid state in which damaged cells release thyroid hormone. More predominant in females 5:1. Begins with a goiter and progresses to hypothyroidism. Grave s disease is hyperthyroid and will eventually burn out the thyroid. If you survive the hyperthyroidism that is. Results in hypothyroidism. Goiter is an enlarged thyroid gland. Often assoc d with hypo (or early Hashimodo s and the hyper state). Lithium drug can interfere with iodine metabolism. Bipolarism is sometimes prescribed this drug. Antithyroid drugs can also impair thyroid production of T4. Used in Grave s prior to surgery or radio therapy to solve the problems. Iodine deficiency is another cause of hypothyroidism. Rare in the US. And of course, thyroidectomy. Secondary: disorders of pituitary Tertiary: disorders of hypothalamaus. Page 3 of 9

4 Hyperthyroidism. Excess production of thyroid hormone. Causes: Grave s disease (most common) Hyperthyroidism, goiter, and often exophthalmos (Marty Feldman eyes). Can actually have it without antithyroid antibodies, but the antibodies are indeed the most common cause. (see slide 16). Also, there are people with exophthalmos who don t have thyroidism. Multinodular goiter Benign adenoma Iodine. Manifestations Mostly from hypermetabolic state and increased sympathetic activity but not true of Grave s disease. Nervousness, irritability, fatigue, weight loss Tachycardia, palpitations, SOB, sweating, muscle cramps, heat intolerance. Tremors, restlessness Goiter, exophthalmos Disorders of the Adrenal Cortex 2 nd most important gland made of: adrenal cortex + adrenal medulla Adrenal cortex creates mineralocorticoids, most important of which is aldosterone, glucocorticoids (making cortisol), sex steroids (testosterone, progesterone, DHEA s) Don t have to know how the hormones are broken down, but know the purpose: Aldosterone hold on to salt. Hyperaldosterone leads to fluid accum, high BP, salt retention. Glucocorticoids (aka, cortisol). Cortisol also causes salt/fluid retention, but is also a modulator of fatty acid metabolism. Helps us hold on to fats and glucose. Balances insulin. Too much cortisol can result in trunk fat and a back hump of fat. Cortisol helps regulate inflammatory reactions. Deficiency of adrenal cortex: Addison s disease, which is adrenal failure is the destuction of the adrenal gland. Can be due to infection or due to other causes. Cushing s is corticoid excess. Page 4 of 9

5 Addison s Disease Mineralocorticoid deficiency from the destruction of all layers of the adrenal cortex. Increased urinary loss of sodium, decreased excretion of potassium (hyperkalemia). Causes dehydration, weakness, fatigue, cardiovascular collapse and shock when severe. Destruction of the cortex is due to autoimmune destruction, infection, cancer, hemochromatosis among others. Secondary insufficiency of adrenal cortex result from hypopituitarism. Results from surgery, tumor, etc. Tertiary insufficiency results from a hypothalamic defect. Longterm corticosteroids (more than 2 weeks and usually prednisone) use results in tertiary insufficiency. Most common cause is long-term administration of corticosteriods with abrupt withdrawl/cessation of drug. Cushing s This is an excess cortisol production. More common. ACTH (adreno-corticotropic hormone) producing tumors in pituitary are more common than something causing an ACTH deficiency. Actually, can be pituitary, adrenal, ectopic, or iatrogenic causes. See slide 29. Iatrogenic produced cushing s (like long term prednisone use) can = osteoporosis. See 30 for more fun manifestations) Cortisol is a modulator of the immune system longterm extra acth = bad immune function. Cushing s = hypokalemia (potassium too low) and hypernatremia (too much sodium) the opposite of addison s. See slide 31. Conn s Syndrome This is an excess of aldosterone, often from a benign adenoma in one of the adrenal cortexes. Page 5 of 9

6 Pancreas So far we ve talked about hypothalamus, pituitary, adrenal cortex. There s also pineal, sex stuff. Pancreas produces Insulin causes glucose to enter the cells so it can be metabolized. Cells have insulin receptors. glucagon (increases glucose in the blood - stimulates liver to breakdown proteins and turn them into useable fuel) catecholamines (stimulate the degradation of fat to produce fuel. These are hormones produced in the adrenal medulla which speed up the production of glucose) adrenaline, epinephrine, norepinephrine, etc. Diabetes Due to an imbalance between the need for insulin and it s available. In Type I, juvenile type, there is often an insufficiency or lack of insulin. Destruction of pancreatic beta cells is often the problem. Used to be called juvenile onset diabetes. Don t believe slide 37 not usually a total lack of insulin, but deficiency. Most cases of Type I are autoimmune caused. Type I manifests with weightloss due to fat utilization and protein for metabolic energy In Type II, the main problem is insulin resistance patients have insulin, but receptors on the cells are insulin insensitive. Can have diminished insulin levels, but more often is the insulin resistance. As a result, there s often too much insulin in the blood. Can also have a hepatic increase of glucose production. The most common risk factor is obesity, followed by age. Type II is often characterized by obesity. How the patient is typed for diabetes changes, apparently frequently. Has been whether person needs insulin supplementation. Type I needs it, type II doesn t. Now some creative mother f er has evidently morphed this in some way that isn t really making it through to my brain. Shit, man. Oh well. Whatchagonnado? Metabolic Syndrome or Syndrome X obesity, diabetes (type 2), hyperlipidemia go into the triad of badness of Metabolic Syndrome. Clinical manifestations of diabetes consist of polyuria (lots of peeing), polydipsia (high thirst), polyphagia (excessive hunger). Those are the classic ones. Can also express with blurred vision fro the hyperosmolar changes in the lens and retina of the eye, chronic skin infections, and yeast infections (vagina in women, foreskin in men). Also expresses in the Type I and II descriptors above. Silly side note: Old school dudes in the west actually tested for it by tasting the urine for sweetness. Old school dudes in China were smarter put it outside to see if the ants went for it. So dead old school western dudes are doing big time after-life head-smacks wishing they had thought of that method. Page 6 of 9

7 Complications of diabetes include DKA (diabetic ketoacidosis), hyperosmolar hyperglycemic state (high concentration of dissolved substances in this case glucose in the blood), and hypoglycemia (low blood sugar). Too much glucose in the blood affects the body in negative ways and I m gonna trust you guys just to read about it. Jerk. DKA: Hyperglycemia osmotic diuresis leading to loss of fluids and electrolytes. The metabolism of fatty acids leads to a high production of ketones, which lowers the ph causing acidosis and cessation of enzyme function. Diabetic ketoacidosis can result in diabetic coma if not sufficiently treated and insulin is insufficient. As blood glucose climbs body produces ketones which are breakdown products of fat which produce the acidosis ph in the blood actually drops. As this develops can result in coma. So this isn t really a direct effect of high blood sugar, but a result of ketone buildup. The hyperosmolar state above refers to hypersaturation of solutes in the blood. This is filtered out by the kidneys and results in peeing a lot. Lose a lot of electrolytes esp sodium and potassium. That s what makes them thirsty. Hypoglycemia is only a complication in treated diabetes. Insulin overdose. Also can be insulin reaction, insulin shock, hypoglycemic coma. Occurs mostly in type I, can be in type II. Onset is rapid. Neuropathy, another exciting complication of diabetes, can be both somatic and autonomic. Somatic is commonly the loss of sensory function stockings and gloves areas. Often loss of sensation to vibration (which usually goes first this is what docs are testing for when they use tuning forks on the extremeties this sensation is carried on the posterior neurological columns, the longest ones in the body which are affected first usually), pain and temperature. Predisposes the person to tissue trauma and diabetic foot ulcers. Healing is very slow which makes infection risk that much higher. Peripheral neuropathy is rather painful. Autonomic include stuff like inadequate autonomic control of gastrointestinal function. Loss of bowel function is rather common get constipation a lot along with impaction. Neuropathy is the leading cause of the end-stage renal disease in the US. Glomerulosclerosis (another name for glomerulonephritis) is a usual expression of renal disease. One of the 1 st manifestations is the appearance of microalbuminuria (leakage of small amount of protein), an early warning of kidney problems. Check diabetics for this often! Remember that blood in the urine can show this way too. Gotta check for blood if no blood but still protein, uh-oh. Can also decrease glomerulofiltration rates, still causing kidney problems. Retinopathy Abnormal vascular permeability. Also, neovascularity and microaneurysims. If you look at the retina, you see little spots of blood/red followed by little trails of red these are called flame hemorrhages which are nearly diagnostic of diabetes. This is what slide 52 means by retinal hemorrhage. These are chagnes in tiny blood vessels. Macrovascular complications Page 7 of 9

8 Affect of the larger vascular system. Can be coronary artery disease, cerebrovascular disease, and peripheral vascular disease (atherosclerosis in the peripherals arms/legs, but legs are the more severe problem). Speeds up plaque formation through several means. On slide 53 the risk factors mean you re more likely to have macrovascular complications as a diabetic if you have that list. Glucose sticks to stuff leads to the formation of glycoproteins causing structural defects of basement membranes of capillaries and arterioles. Micro and macrovascular complications by the way are the reason diabetics have such problems healing nutrients don t get to the wound to heal, high glucose levels feed bacteria, waste products don t go away easily. Essay question: Describe the affects of diabetes. Focus on nerves and how high blood sugar affects nerves, risk of coronary artery disease, and how it affects the retina of the eye, and how it affects the immune system. Address the distinctions between insulin dependence and non-insulin dependent diabetes. See slide 47 as a guide micro and macroangiopathies affecting small and large vessels. Spend some time researching that. (sure. Like I have time.) Gestational Diabetes This is the weird 3 rd type diabetic while preggers. Family history, obesity, advanced maternal age are all risk factors. History of spontaneous abortion is another as is LGA babies (LGA=large for gestational age). 5+ pregnancies is another risk factor. Complications = placental insufficiency leading to impaired growth and stillbirth. Another complication is fetal macrosomia (i.e., damn! That s a big baby!) due to the excess glucose. Toxemia on slide 57 is hypertension in a pregger. Oral hypoglycemics are not used in gestational diabetes because they cause birth defects. Slide 59. Instead, treated with diet changes and insulin when necessary. Obviously nutritional changes are best low glycemic foods and complex carbos, protein with lots of veggies, no dairy/fat/simple carbos. Chromium can help as does weight loss. And that s the last slide we re responsible for. TK, fyi, it s 5:20 and we re still here. He s pontificating (definition: To speak in a patronizing, supercilious or pompous manner, especially at length. ). One more essay on the next page Page 8 of 9

9 Essay Question: Describe the following compare and contrast: tension headache migraine headache cluster headache mixed headache Page 9 of 9